Effects of Taurine and Structurally Related Analogues on Ca²⁺ Uptake and Respiration Rate in Rat Liver Mitochondria

Abstract

Mitochondria from vertebrate sources possess an elaborate system for transporting Ca²⁺ across their inner membrane. This process includes accumulation of the cation into their matrix, via an uniporter mechanism. This is balanced by electroneutral Ca²⁺ release mediated by the functioning of a 2 Na⁺:1 Ca²⁺ exchanger or “antiporter” in mitochondria from most tissues, including heart, brain and brown adipose tissue, or by a 2H⁺/Ca²⁺ antiporter in liver⁷. In addition to these functions, mitochondria produce about 95% of the common cellular energy as ATP by means of oxidative phosphorylation. Under physiological conditions, Ca²⁺ transport and energy production seem to be strictly correlated and there is convincing evidence that the intramitochondrial Ca²⁺ concentration functions as a metabolic control in signalling the mitochondria to modify its metabolic rate in response to increased energy demand. According to the theory of flux control, the steps of Ca²⁺-mediated metabolic control are distributed and include activation of the Ca²⁺-sensitive dehydrogenases^{2, 9} and other Ca²⁺-sensitive metabolic processes^{8, 16}. In this context, drugs that alter the flux of Ca²⁺ across mitochondrial membranes could, in theory, play a role in modulating the cellular energetic metabolism.